This invention relates to an implantable cardioverting/defibrillating pacemaker and, more particularly, to a pacemaker of this type which has the ability to sense haemodynamic compromise in a patient's heart. This ability, when incorporated into an automatic implantable arrhythmia control system, is used for the determination of tachyarrhythmias and acts as a trigger for the automatic delivery of antitachycardia pacing, cardioversion and/or defibrillation therapy.
Pacemakers were initially developed to electrically stimulate hearts that were unable to beat at a rate sufficient to maintain a life sustaining cardiac output. The first devices delivered electrical stimuli at a fixed rate, regardless of the heart's function or the body's physiological needs.
Devices were then developed that stimulated the heart only if it failed to beat above a predetermined rate. Such devices sensed the electrical activity of the heart, usually in the right ventricle. Later developments saw the introduction of pacemakers that sensed and stimulated in both the right atrium and right ventricle.
Pacemakers with the ability to sense the physiological demand for an increase in heart rate were then introduced. One example of this is disclosed in U.S. Pat. No. 4,702,253, to Nappholz et al., wherein the device determines physiological demand by the sensing of respiratory minute volume, and increases the pacing rate in response to increases in minute volume.
Devices were developed that electrically sensed the presence of a ventricular tachyarrhythmia and delivered a defibrillating DC shock to revert the heart to a normal rhythm. More advanced devices where developed that paced hearts undergoing a tachyarrhythmia back into normal rhythm.
Recent technology has brought about the development of automatic implantable arrhythmia control systems. These devices are able to pace a heart that is beating too slowly, to cardiovert/defibrillate a fast tachyarrhythmia and to pace a heart undergoing a slower tachyarrhythmia back into a normal rhythm. One such device is disclosed in the U.S. Pat. No. 4,940,054 of Grevis et al. The Grevis et al. device comprises a microprocessor-based arrhythmia control system. It has the capability of being reprogrammed, while implanted, via an external programmer and a radio frequency telemetry link. The use of a telemetric link allows not only the reprogramming of the device but also the interrogation of the device by a clinician. Various parameters, such as bradycardia pacing rate and amplitude, antitachycardia pacing algorithms and cardioversion and defibrillation energies, can be re-programmed to suit the needs of the recipient of the device.
There are limitations inherent in devices of the above type as they rely solely upon the sensing of the electrical activity of the heart as the means of determining the state of cardiac function. Also, there is a possibility that the device may be confused by electrical noise induced in the sensing circuits and causing difficulty in distinguishing a supraventricular tachyarrhythmia (SVT) from a ventricular tachyarrhythmia (VT). Furthermore, although having the ability to detect tachyarrhythmias, such devices are unable to determine whether or not the detected tachyarrhythmia is haemodynamically compromising, regardless of its origin.
It has been shown that there are differences in the haemodynamic effects of the different tachyarrhythmias. This has been documented by Nakano in his article "Effects of Atrial and Ventricular Tachycardias on the Cardiovascular System", Am. J. Physiol., Vol. 206, pages 547-552 (1964). Hence, the application of certain selected therapies may be haemodynamically inappropriate. An example of such a shortcoming is that a patient suffering from a haemodynamically compromising slow VT may be subject to the inappropriate delivery of antitachycardia pacing therapy (ATP), instead of defibrillation therapy. Conversely, a VT may not necessarily be haemodynamically compromising and therefore not require ATP therapy, yet ATP therapy may automatically be delivered by the device.
U.S. Pat. No. 4,730,619, to Koning et al., discloses that the impedance between the ring and tip electrodes of an implantable cardiac pacing lead can be used as measure of cardiac output. This patent uses that measure of cardiac output to optimize the function of a bradycardia support pacemaker. The Koning et al. device is limited in that its application is only for bradycardia support pacing. There is no means disclosed for antitachycardia pacing or cardioversion/defibrillation, nor any method to detect the onset or presence of haemodynamically compromising arrhythmias. Also, the means of sensing the impedance is restricted to the use of the ring and tip electrodes of a bipolar implantable cardiac pacing lead.
U.S. Pat. No. 4,733,667, to Olive et al., discloses a method for closed loop control of cardiac stimulating utilizing rate of change of impedance. Olive et al. use a fixed quadripolar electrode to derive an intracardiac impedance signal to drive a rate responsive bradycardia support pacemaker. Their device is not capable of delivering antitachycardia pacing, nor defibrillation therapy, nor was it designed to recognize haemodynamically compromising arrhythmias.
U.S. Pat. No. 4,702,253, to Nappholz et al., discloses a pacemaker and method of using the same to determine minute volume. In this device the transthoracic impedance is measured and used as a means of determining the respiratory minute volume. It senses the transthoracic impedance between its case and the tip electrode of the ventricular lead. The injected current is passed between the ring electrode of the ventricular lead and the case. Filtering is used to specifically remove the changes in impedance due to the action of the heart. This device is a rate responsive bradycardia support device that specifically filters out the cardiac impedance signal. The patent does not disclose a method to detect haemodynamically compromising arrhythmias, nor the means for delivering antitachycardia pacing nor defibrillation therapy.
U.S. Pat. No. 4,291,699, to Geddes et al., discloses a method and apparatus for automatically detecting and treating ventricular fibrillation. Geddes et al. use the intracardiac impedance sensed between two electrodes mounted upon a permanently implanted intracardiac catheter as a means of confirming the presence of ventricular fibrillation (VF). In the Geddes et al. device the endocardial lead is placed in only one ventricle. It is therefore limited in that it at best accounts for only a part of the volume changes and hence only a portion of the mechanical pumping activity of one ventricle. It also fails to determine the mechanical pumping activity of the other ventricle, and as such is not an accurate measure of haemodynamic compromise. Examples of this shortcoming are when a patient's AV valve fails to close completely, or when there exists the condition of high vascular resistance in the lungs. It is believed that as a result of this there is a large weighting of the electrical aspect of detection.
Our research has shown that the Geddes et al. system is very subject to the positioning of the electrode, especially the tip of the electrode. The endocardial surface of the human ventricle is corrugated. The endocardial rugae and valvular tendineae provide multiple locations in which an electrode may lodge. However, the positioning of an electrode tip within such a corrugation can lead to errors in the measurement of impedance.
The human cardiac tissue has a relatively similar impedance to that of blood. Therefore, changes in blood volume to both of the ventricles of the heart form a large part of the overall impedance between patch electrodes, allowing for blood volume changes to be easily measurable.
If the electrode tip as disclosed in Geddes et al. is sited in a deep rugae, that is, in what is effectively a "well" within the surface of the endocardium, the proportional blood volume changes and hence impedance changes would be considerably lower and therefore more difficult to measure. Also it would be more difficult to accurately measure smaller amounts of impedance changes relating to the higher levels of haemodynamic compromise, as in VT/VF.
The performance of devices that sample intracardiac impedance signals has proven to be subject-variable, with some electrode configurations working in one subject but not in another. In the device of Geddes et al., therapy decisions are made upon the weighted ANDing of right ventricular impedance and rate criteria, with the facility to ignore the impedance signal if its use proves problematic. It has been found by the present inventor that the means of overcoming this problem is to measure the required impedance signal across both the left and right ventricles of the heart. An added feature of my invention is to perform the impedance measurements from the outside of the heart.
Accordingly, it is a primary object of the present invention to provide a device capable of measuring haemodynamic compromise in both ventricles of the patient's heart by determining the changes in normal variations of the transcardiac impedance between defibrillator patches placed on the outer surface of the patient's heart.
An additional object of the invention is to provide a device capable of classifying and detecting tachyarrhythmias according to discrete levels of haemodynamic compromise sensed by the device.
Yet another object of the invention is to provide a safe reliable device capable of delivering appropriate antitachyarrhythmia therapy according to the discrete level of haemodynamic compromise sensed by the device.
Further objects and advantages of the invention will become apparent as the following description proceeds.